> Disease Condition

Post myocardial infarction treatment has previously seen decades of failure.

No current treatment is able to prevent the death of cardiomyocytes and a reduction in lifespan and quality of life.

“Still there is no therapy aimed at reducing injury that is clearly associated with improved clinical outcomes”

European Society of Cardiology
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Current Treatment

Our emergency health services are excellent at treating myocardial infarction (MI) in the acute phase via percutaneous coronary intervention (PCI) “Stent”, however the long-term prognosis of MI remains very poor.

> Whilst a range of drugs exist, they only act to slow progression of heart failure and somewhat reduce likelihood of future major heart problems.

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Myocardial Infarction

Current Standard of Care

01.
Emergency Transfer
to Hospital
02.
Reperfusion by Percutaneous Coronary
Intervention (PCI) “Stent”
03.
Long-term pharmacotherapy
+ Scarring & Failure
04.
Reduction in lifespan
and quality of life
Ischemia

Inadequate blood flow to the heart (ischemia), as occurs during heart disease, causes physiological stress to cardiac cells.

Stress lasting more than approx. 30 mins causes death of the cells and lasting damage whereas reversal of ischemia within this period preserves cellular function.

In the US the median time from MI symptoms to treatment (usually PCI) is 185 mins, meaning most patients experience inevitable irreversible damage, with damage increasing in those patients with delayed time to PCI.

>30+

min ischemia

Cell death + lasting damage

0-30

min ischemia

No lasting damage

Cardiac Function

Cardiac functional reserve is the difference between peak (i.e. maximal stress at peak exercise) and baseline resting values. 

Cardiomyocyte death reduces normal heart fitness and lifespan after MI.

Cardiac functional reserve is the difference between peak (i.e. maximal stress at peak exercise) and baseline resting values. With increasing age, natural attrition results in progressive diminution in the pumping capability of the heart and cardiac reserve, while baseline resting cardiac function (dashed horizontal line) remains largely unchanged.

With discrete incidences of cardiomyocyte loss through myocardial infarctions pumping capability plummets stepwise with each incident. When this falls below the normal baseline level, a state of extreme cardiac failure (cardiogenic shock) ensues, which is rapidly followed by death unless drastic measures (e.g. surgery) are successful.

The accelerated deterioration of cardiac pumping capability (secondary to putative myocyte attrition) can be ameliorated with neurohumoral therapies.

(Adapted from Exp Physiol 2003 883. 447-458)
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Myocardial Infarction

Revolutionising Treatment After MI

01.
Emergency Transfer
to Hospital
02.
Forcefield Revolutionary
Treatment + “Stent”
03.
Preserved Function
+ Reduced Scarring
04.
Extended Life
and Healthspan

Forcefield Therapeutics is pioneering three proteins with the natural ability to retain heart function after myocardial infarction, by preserving cardiomyocytes, sustaining cardiac function and preventing clinical changes in the heart.

Forcefield has the potential to revolutionise acute post-myocardial infarction treatment which has previously seen decades of failure. We are adding to the toolbox that health professionals can use, improving outcomes and reducing the reliance on long term medication.

Treatment